Transportation noise pollution as a cardiovascular risk factor: from epidemiological evidence to mechanistic insights.

Abstract

Transportation noise from road, rail, and aircraft traffic is now recognized as a major cardiovascular risk factor. In Europe, more than 113 million people are chronically exposed to levels above 55 dB(A), resulting in an estimated 1.3 million healthy life-years lost annually from traffic-related noise. Large epidemiological studies consistently demonstrate associations with ischemic heart disease, heart failure, stroke, and type 2 diabetes, with additional links to hypertension, atrial fibrillation, and obesity. Translational and experimental research has clarified the biological plausibility of these findings. The central "noise reaction model" involves activation of the sympathetic nervous system and hypothalamic-pituitary-adrenal axis, with subsequent release of catecholamines and cortisol. These stress responses provoke endothelial dysfunction, vascular inflammation, and oxidative stress, largely through NADPH oxidase 2 activation and nitric oxide synthase uncoupling. At the molecular level, noise alters gene expression networks, disrupts circadian clock regulation, downregulates FOXO3, and induces pro-inflammatory epigenetic modifications. Neuroimaging studies reveal chronic noise activates the amygdala, linking stress perception to vascular inflammation and major adverse cardiovascular events. Adverse effects are most pronounced at night, when noise fragments restorative sleep and amplifies neurohormonal imbalance. Importantly, these pathways overlap with mechanisms of traditional cardiovascular risk factors - diabetes, hypertension, smoking, and hyperlipidemia - suggesting that noise accelerates vascular aging through convergent mechanisms. Combined exposure to noise and air pollution further exerts additive or synergistic effects, underscoring the value of the exposome concept in identifying vulnerable populations. Transportation noise should therefore be considered an established cardiovascular risk factor, requiring equal priority in prevention guidelines and public health policy. See also the graphical abstract(Fig. 1).